|
|
 |
|
ORIGINAL ARTICLE |
|
Year : 2023 | Volume
: 20
| Issue : 1 | Page : 71-76 |
|
Relationship of serum ghrelin, amylase and lipase with insulin level in type 2 diabetes mellitus patients
Zahraa Raad Abdulhakeem, Atheer Hameid Odda, Sura Ahmed Abdulsattar
Department of Chemistry and Biochemistry, College of Medicine, University of Kerbala, Karbala, Iraq
Date of Submission | 25-Oct-2022 |
Date of Acceptance | 07-Nov-2022 |
Date of Web Publication | 27-Apr-2023 |
Correspondence Address: Zahraa Raad Abdulhakeem Department of Chemistry and Biochemistry, College of Medicine, University of Kerbala, Karbala Iraq
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/MJBL.MJBL_255_22
Background: Diabetes mellitus (DM) is a metabolic disorder known as hyperglycemia, which is brought on by impaired insulin secretion, inefficient insulin utilization, or both. Objectives: This study’s aim was to assess the lipase and amylase amylase pancreatic enzymes levels in sera of (T2DM) patients and healthy control subjects. Materials and Methods: A case-control research was conducted from December 2021 to March 2022 at the Hilla District Center for Diabetes and Endocrinology in Babylon, Iraq.It included a group of 39 patients with type 2 DM and 39 healthy people between the ages of 35 to 60 years. Results: Results were indicating a significant difference in FBS among groups, The mean levels of FBS for DM was (203.7 ± 72.3) mg/dL which was significantly greater than it was for the control group (88.6 ± 7.64) mg/dL,(P ≤ 0.001). The mean of HbA1c for DM (9.5 ± 2.35) was significantly higher than for control (4.9 ± 0.48), P ≤ 0.001.The mean levels of the Amylase and Lipase activity in the DM patients group were (71.4 ± 29.11) and (49.7 ± 14.69) (U/L). When compared to the control group’s mean values, which were (72.7 ± 27.19) and (42.0 ± 7.35) (U/L). The mean levels of Lipase activity were shown a significant difference in T2DM patients compared to the healthy control group, (P < 0.05). Conclusion: Increased serum level of lipase without any symptoms of pancreatitis was indicated in type II diabetes mellitus patients. Keywords: Amylase, diabetes mellitus type 2, FBS, HbA1c, lipase
How to cite this article: Abdulhakeem ZR, Odda AH, Abdulsattar SA. Relationship of serum ghrelin, amylase and lipase with insulin level in type 2 diabetes mellitus patients. Med J Babylon 2023;20:71-6 |
How to cite this URL: Abdulhakeem ZR, Odda AH, Abdulsattar SA. Relationship of serum ghrelin, amylase and lipase with insulin level in type 2 diabetes mellitus patients. Med J Babylon [serial online] 2023 [cited 2023 Jun 10];20:71-6. Available from: https://www.medjbabylon.org/text.asp?2023/20/1/71/375124 |
Introduction | |  |
Diabetes mellitus (DM), which is brought on by ineffective insulin production, inefficient insulin utilization, or both, is the result of the metabolic disorders known together as diabetes mellitus (DM).[1],[2] (DM) is characterized by immune-mediated (Type 1 diabetes), insulin resistance (Type 2 diabetes), gestational hyperglycemia, or other chronic hyperglycemia; genetic, environmental, infectious, or medication-induced problems; or affects the beta cells of the islets of Langerhans.[3],[4],[5] No country is safe from the diabetes invasion these days since type 2 diabetes mellitus (T2DM) is a significant public health concern or threat in the twenty-first century.[6] Compared to the proportion of 4.6% in 2000, it is predicted that the anticipated global prevalence of T2DM will rise to 6.4% in 2030. Over the past decade, the prevalence of diabetes has risen rapidly due to an increase in the average age of the community, hereditary background, unhealthy dietary habits, sedentary lifestyle, and increased obesity in line with the growth of urbanization.[7] The increasing prevalence of type 2 diabetes in general and in younger people in particular had led to an increasing number of pregnancies with this complication.[8]
Hyperglycemia develops as the disease develops because insulin secretion can no longer keep glucose levels under control. Patients with T2DM are typically obese or have greater body fat percentages, which are primarily distributed in the abdomen area. Adipokine dysregulation and a rise in the production of free fatty acids are two inflammatory mechanisms used by adipose tissue to enhance insulin resistance in this condition (FFA).[9]
Population aging, sedentary lifestyles, high-calorie diets, and the global growth in obesity have all contributed to a four-fold increase in the incidence and prevalence of T2DM.[9],[10] Overall, men are more likely than women to have diabetes, and individuals 40 and older are the group most likely to have the disease. Additionally, T2DM is becoming increasingly common in adolescents and young adults more quickly. The top five nations with the highest prevalence of T2DM are Japan, Indonesia, China, India, and the United States.[11],[12]
According to a recent study, diseases like “diabetes mellitus” that have subclinical reduction of exocrine pancreatic function frequently have lower serum concentrations of pancreatic enzymes.[13] The most important enzyme for breaking down dietary fat, decreasing the buildup of fat in adipose tissue, and regulating weight gain is pancreatic lipase, all of which have positive effects on overweight and obesity, which are common in diabetes patients. Triglycerides, which make up 90 to 95% of the ingested fats, are broken down and absorbed by pancreatic lipase. The use of a lipase inhibitor was previously considered as an obesity treatment if there is a way to stop the early transfer of triglycerides from the intestinal lumen. Orlistat, a hydrolyzed version of the lipase inhibitor lipstatin derived from Streptomyces toxitricini, is a potent inhibitor of gastric, pancreatic, and carboxyl ester lipase. In treating obesity, a major risk factor for type 2 diabetes, it has showed potential.[14] The level of C peptide and pancreatic enzyme activity have been found to be significantly correlated by research.[15] This distinction might be explained by the fact that trypsin is the first enzyme to be lost in the sequence of enzyme loss in the exocrine pancreatic damage linked to human diabetes, and lipase is the last.[16]
The majority of studies have concentrated on the metabolic disturbance brought on by reduced insulin action and prolonged hyperglycemia. Malnutrition and maldigestion can result from altered pancreatic endocrine activity, amylase, diabetes mellitus, and altered pancreatic endocrine activity. The current study aims to assess exocrine pancreatic function in type 2 diabetics by measuring blood amylase and lipase levels.[17] In individuals with diabetes mellitus, hyperglycemia and/or insulin inactivity brought on by hypoinsulinemia or insulin resistance may result in pancreatic exocrine dysfunction and the emergence of pancreatic exocrine insufficiency.[18]
Materials and Methods | |  |
Patients and controls
The Center for Diabetes and Endocrinology of Hilla District, Babylon, Iraq, conducted a case-control study from December 2021 to March 2022 for the current study. 39 patients with type 2 diabetes and 39 healthy individuals between the ages of 35 and 60 made comprised the study’s patient and control groups. Age, gender, and BMI were among the sociodemographic characteristics that were gathered using a self-reporting technique (study questionnaire). Patients with type 2 diabetes mellitus, who made up 50% of the patient population and had an average age of (35 to 60) years, were included. Diabetes symptoms include frequent urination, intense hunger or thirst, excessive fatigue, blurred vision, wounds or bruises that take a long time to heal, and tingling, discomfort, or numbness in the hands or feet, according to the American Diabetes Association (ADA). Doctors have identified this problem in each case (type 2). About 50% of the participants in the control group were healthy people. None of the individuals showed any disease-related symptoms or indications. Patients with the following conditions were excluded from the study: smokers, pregnant women, Type 1 diabetics, chronic liver disease, heart disease, hypertension, and insulin medication dependency. Quantitative determination of α-amylase in serum was done by kinetic method (CNPG3) and the fasting serum glucose, serum lipase was determined by the colorimetric approach. The turbid metric inhibition immunoassay (TINIA) for hemolyzed whole blood was used to determine the HbA1c level.
Ethical approval
The study was conducted in accordance with the ethical principles that have their origin in the Declaration of Helsinki. It was carried out with patients verbal and analytical approval before sample was taken. The study protocol and the subject information and consent form were reviewed and approved by a local ethics committee according to the document number 1050 (including the number and the date in 23/5/2022) to get this approval. The Kerbala Medical College Ethical Committee and the Committee of the Endocrinology Unit of the Center of Diabetes and Endocrinology of Hilla District, Babylon, Iraq, both gave their approval to the study protocol. After receiving patients’ or patients’ families’ agreement, samples were taken.
Result | |  |
Diabetes mellitus (DM) prevalence is rapidly and steadily increasing worldwide. Diabetes used to be considered a minor disease that mostly affected elderly people, but over the past three generations, it has gained more attention and is now one of the leading causes of morbidity and mortality in middle-aged and young people. Chronic diseases are brought on by functional decline brought on by high blood sugar, insulin sensitivity, and insulin shortage.[19]
Clinical and demographic characteristics
The clinical demographics of the patients’ group were summarized in [Table 1]. Table illustrated the age range of analysed group which was within (36–59) Years for patients and (31–58) Years for healthy control group. The gender distribution was nearly similar in both groups; mostly of the participants were not smokers. The minimum duration the diabetes was five years; about 56% having Family History of DM and 54% were suffering from hypertensive. More than half of the patients were reporting to use Glucophage and Insulin as a regular medication. | Table 1: Baseline characteristics and demographic descriptive of the study population in cases of DM patients
Click here to view |
Fasting blood sugar
Generally, patients with type II diabetes mellitus patients were shown an increasing range level of FBS when compared to the healthy control groups. Results were indicating a significant difference in FBS among groups, The means, and standard deviations were presented in [Table 2]. The mean level of FBS for DM was (203.7 ± 72.3) mg/dL which was significantly greater than for control group (88.6 ± 7.64) mg/dL, (P ≤ 0.001). The Distribution of serum levels of fasting blood sugar in type II diabetes mellitus patients compared to healthy control group was presented in [Figure 1]. | Table 2: Descriptive statistics and mean difference of biomarkers level in type II diabetes mellitus patients compared to healthy control group
Click here to view |  | Figure 1: Boxplot of the serum level distribution of (FBS, HbA1c, amylase, lipase) in type II diabetes mellitus patients compared to healthy control group
Click here to view |
Hemoglobin A1C
The hemoglobin A1c (HbA1c) was also examined. The mean levels of serum HbA1c in DM patients were significantly higher than those of healthy individuals (P < 0.05), as illustrated in [Figure 1] and [Table 2]. The mean of HBA1C for DM (9.5 ± 2.35) was significantly higher than for Control (4.9 ± 0.48), P ≤ 0.001.
Serum pancreatic enzyme (amylase) activity (U/L)
The distribution of serum pancreatic enzymes (amylase) was examined as demonstrated in [Figure 1]. Generally, patients with Type II Diabetes Mellitus were shown an increasing range level of pancreatic enzymes when compared with the healthy control groups. Mean levels of amylase activity in DM patients group were (71.4 ± 29.11) (U/L) whereas the mean values in the control group were (72.7 ± 27.19) (U/L). Lipase activity was shown a significant difference in type II diabetes mellitus patients compared to healthy control group, (P < 0.05).
Serum pancreatic enzymes (lipase) activity (U/L)
The distribution of serum pancreatic enzymes (lipase) was examined as demonstrated in [Figure 1]. Generally, patients with type II diabetes mellitus were shown an increasing range level of pancreatic enzymes when compared with the healthy control groups. Mean levels of lipase activity in the DM patients group were (49.7 ± 14.69) (U/L) respectively, whereas the control group’s mean levels were (42.0 ± 7.35) (U/L).
Correlation analysis
The individual Correlation Coefficients of the lipase, and amylase were presented in [Table 3]. | Table 3: Correlation coefficients of lipase, and amylase and the measured biomarkers in DM patients
Click here to view |
Discussion | |  |
The results for FBS and HbA1c analysis were significant (P < 0.001) and indicated Significant variations in FBS were found between the group [Figure 1] and [Table 2] results indicated that diabetic patients (DM) have a significantly higher sugar profile than the healthy control group. Also, mean levels of serum HbA1c in DM patients were significantly higher than those of healthy individuals (P < 0.05), as illustrated in [Figure 1].
Diabetes is characterized by chronic hyperglycemia and causes long-term complications. Since glycated hemoglobin considers a reflection of integrated glycaemia over the entire 120-day lifespan of the red blood cell, HbA1c levels and FBS have a significant correlation. HbA1c is a helpful tool for managing chronic diabetes since it is a reliable predictor of chronic glycemia and correlates well with the risk of acquiring long-term diabetes.[20] Diabetics have higher blood glucose levels, and glucose binds to hemoglobin in a concentration-dependent method. As hemoglobin becomes glycated with glucose, it forms glucose-bound (glycated) hemoglobin, also known as HbA1c, which measures the average blood glucose levels of a person. It’s crucial to remember that there is an antagonistic relationship between blood sugar levels and HbA1c levels.[21] Type 2 diabetes mellitus (DM), which is brought on by impaired insulin production, has hyperglycemia as one of its symptoms.[22] Understanding insulin and insulin resistance completely is made possible by the relevance of the HbA1c test in the diagnosis and prognosis of diabetes patients. Direct links exist between HbA1c and insulin resistance, with HbA1c being more strongly linked to insulin sensitivity in healthy individuals with normal glucose tolerance.[23]
There are very few human research that have attempted to investigate the biochemical characteristics and underlying mechanisms connecting the exocrine acinar cells and the endocrine islet cells.[24]
An endocrine problem of the pancreas is indicated by diabetes mellitus (DM), a metabolic illness marked by hyperglycemia and linked with insulin insufficiency or resistance. Enzymes like lipase and amylase are secreted by the pancreas’ exocrine part. Diabetes-related endocrine dysfunction may affect the pancreas’ exocrine function. As a result of poor insulin action brought on by either insulin resistance or insufficient insulin secretion, reduced serum amylase levels in diabetes were also linked to higher blood glucose levels (negative association).[24] According to Patel R et al., decreased amylase secretion in the diabetic pancreas may be brought on by a decrease in the amount of cytosolic free calcium (Ca2+) and amylase gene expression as compared to the gene expression for the receptor cholecystokinin (CCK) in pancreatic acinar cells.[25] Exocrine pancreatic insufficiency has been related to long-term type 2 diabetes (T2D), and T2D patients are more likely to develop acute or chronic pancreatitis. In addition, the main causes of diabetes sequelae such retinopathy, nephropathy, neuropathy, and other conditions are long-term T2D and insufficient glycemic control.[26] A different study found that greater serum levels of pancreatic enzymes (amylase and/or lipase) indicated a higher incidence of pancreatitis.[27] Conditions other than pancreatitis, such as renal illness, hyperglycemia, and ketoacidosis, can exacerbate abnormally high blood lipase activity levels.[28] Although T2DM was linked to an increased risk of pancreatitis, the pathogenic mechanism is yet unknown.[27] The pancreas’ exocrine-endocrine interactions can be impaired by the elevated serum lipase activity found in individuals who have diabetes and prediabetes. Higher lipase activity is linked to both inadequate insulin secretion and poor insulin action due to insulin resistance in both the diabetes and prediabetes groups because insulin promotes enzyme production and release in the exocrine pancreas.[29] Inflammatory pancreatic exocrine disease, often known as pancreatitis, is indicated by increased lipase activity in T2D.[30] An increase in lipase activity, a decrease in insulin levels, an increase in FPG, HbA1c, creatinine, insulin resistance, and a dyslipidaemia profile are all signs of diabetes, according to a previous study (increasing level of total cholesterol, triglyceride, and small dense LDL particles). Based on the study of the fictitious structural model, which demonstrates a significant positive link between the high glucose level and lipase activity, lipase activity does not considerably contribute to the elevation of glucose, nevertheless. As a result, we predict that Indonesian T2D duration or glycemic control impairment are correlated with pancreatitis or a high serum lipase value. Uncontrolled glucose levels can increase triglyceride levels and lipase production, which in turn causes triglycerides to break down into free fatty acids.[31]
The exocrine function of the pancreas may be affected by the endocrine deregulation seen in diabetes. Diabetes patients with low serum amylase levels have higher blood sugar levels (negative correlation), which was brought on by poor insulin action brought on by either insulin resistance or insufficient insulin production. The lack of pancreatic exocrine acinar cells was the cause of the drop in amylase levels.[24]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Egan AM, Dinneen SF What is diabetes? Medicine (United Kingdom) 2019;47:1-4. |
2. | Aronson R, Goldenberg R, Boras D, Skovgaard R, Bajaj H The canadian hypoglycemia assessment tool program: Insights into rates and implications of hypoglycemia from an observational study. Can J Diabetes 2018;42:11-7. |
3. | Baynest HW Classification, pathophysiology, diagnosis and management of diabetes mellitus. J Diabetes Metabol 2015;6:1-9. |
4. | Centers for Disease Control and Prevention. National Diabetes Statistics Report. Atlanta, GA: Centers for Disease Control and Prevention, US Department of Health and Human Services; 2020. https://www.cdc.gov/diabetes/data/statist ics/2014statisticsreport.html. [Last accessed on 23 Jun 2020]. |
5. | Nair M Diabetes mellitus, part 1: Physiology and complications. Brit J Nurs 2007;16:184-8. |
6. | Zimmet P The burden of type 2 diabetes: Are we doing enough? Diabetes Metab 2003;29:6S9-18. |
7. | Abbas ZAE, El-Yassin HD The impact of glycemic control on procalcitonin level in patients with type ii diabetes. Medical Journal of Babylon 2022;19:391. |
8. | Mahmood KS, Abd Al-Rasol EA The effect of Vit B12 deficiency, homocystein, and lipid metabolism in association with increased risk of gestational diabetes mellitus. Medical Journal of Babylon 2022;19:409. |
9. | Chatterjee S, Khunti K, Davies MJ Type 2 diabetes. Lancet 2017;389:2239-51. |
10. | NCD Risk Factor Collaboration. Worldwide trends in diabetes since 1980: A pooled analysis of 751 population-based studies with 4.4 million participants. Lancet 2016;387:1513-30. |
11. | Virally M, Laloi-Michelin M, Médeau V, Meas T, Kévorkian JP, Mouly S, et al. Muscle infarction in a young woman with brittle type 1 diabetes. Diabetes Metab 2007;33:466-8. |
12. | Rathmann W, Giani G Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care 2004;27:2568-9; author reply 2569. |
13. | Dandona P, Elias E, Beckett AG Serum trypsin concentrations in diabetes mellitus. Br Med J 1978;2:1125. |
14. | Savych A, Marchyshyn S Inhibition of pancreatic lipase by water extracts of some herbal mixtures. Methods 2021;20:21. |
15. | Fonseca V, Berger LA, Beckett AG, Dandona P. Size of pancreas in diabetes mellitus: A study based on ultrasound. JBritish Med 1985;29:1240. |
16. | Junglee D, De Albarran R, Katrak A, Freedman DB, Beckett AG, Dandona P. Low pancreatic lipase in insulin-dependent diabetics. Journal of Clinical Pathology 1983;36:200-2. |
17. | Tanvi NEJ, Akhter QS, Nahar S, Sumi MN, Hosen M. Serum amylase and lipase levels in type 2 diabetes mellitus. Journal of Bangladesh Society of Physiologist 2017;12:52-6. |
18. | Nakajima K, Oshida H, Muneyuki T, Kakei M Pancrelipase: An evidence-based review of its use for treating pancreatic exocrine insufficiency. Core Evid 2012;7:77-91. |
19. | Mishra V, Nayak P, Sharma M, Albutti A, Alwashmi ASS, Aljasir, MA, et al. Emerging treatment strategies for diabetes mellitus and associated complications: An update. Pharmaceutics 2021;13:1568. |
20. | Herman WH, Fajans SS Hemoglobin A1c for the diagnosis of diabetes: Practical considerations. Pol Arch Med Wewn 2010;120:37-40. |
21. | Nathan DM, Davidson MB, DeFronzo RA Impaired fasting glucose and impaired glucose tolerance: Implications for care. Diabetes Care 2007 30:753-9. |
22. | Buse JB, Polonsky KS, Burant CF Chapter 31: Type 2 diabetes mellitus. In: Melmed S, Polonsky KS, Larsen PR, Kronenberg HM, editors. Williams Textbook of Endocrinology. 12th ed. Philadelphia, PA: Saunders Elsevier and 1386–450; 2011. |
23. | Lin JD, Chang JB, Wu CZ Identification of insulin resistance in subjects with normal glucose tolerance. Ann Acad Med Singapore 2014;43:113-9. |
24. | Madole MB, Iyer CM, Madivalar MT, Wadde SK, Howale DS Evaluation of biochemical markers serum amylase and serum lipase for the assessment of pancreatic exocrine function in diabetes mellitus. J Clin Diagn Res 2016;10: BC01-4. |
25. | Patel R, Atherton P, Wackerhage H, Singh J Signaling proteins associated with diabetic-induced exocrine pancreatic insufficiency in rats. Ann N Y Acad Sci 2006;1084:490-502. |
26. | Ewald N, Hardt PD Diagnosis and treatment of dia- betes mellitus in chronic pancreatitis. World J Gastro- enterol 2013;19: 7276-81. |
27. | Srihardyastutie A, Soeatmadji DW, Fatchiyah AA Relation of elevated serum lipase to Indonesian type 2 diabetes mellitus progression. Biomed Res 2015;26:293-8. |
28. | Amandeep Kaur NV Proteomics: A hallmark tool for identification of biomarker (LIPASE) in type I & II diabetes mellitus patients. Adv Appl Sci Res 2012;3:1842-47. |
29. | Andren-Sandberg A, Hardt PD Workshop report: Giessen international workshop on interactions of ex- ocrine and endocrine pancreatic diseases. J Pancreas 2005;6:382-405. |
30. | Beauregard JM, Lyon JA, Slovis C Using the literature to evaluate diagnostic tests: Amylase or lipase for diagnosing acute pancreatitis? J Med Libr Assoc 2007;95:121-6. |
31. | Srihardyastutie A, Soeadmadji DW, Fatchiyah F, Aulanniam A Lipase/amylase ratio as the indication of pancreatic exocrine inflammation and the correlation with insulin resistance in type 2 diabetes melli- tus. In: Proceeding of the 4th Annual Basic Science International Conference. (BASIC) 2014:33-7. |
[Figure 1]
[Table 1], [Table 2], [Table 3]
|